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Fig. 5 | Clinical Epigenetics

Fig. 5

From: DNA methylation in human gastric epithelial cells defines regional identity without restricting lineage plasticity

Fig. 5

Differential methylation in intestinal metaplasia. A Enrichment of hypermethylated and hypomethylated CpGs in TF binding sites (JASPAR collection) in organoids derived from intestinal metaplasia (IM) biopsies compared to organoids derived from normal gastric biopsies. Shown are log odds ratios of significantly enriched (log odds ratio > 0.6) or depleted (log odds ratio <  − 0.6) genomic features (FDR < 0.05). Color code ranges from blue (depleted) to red (enriched); gray refers to a log odds ratio between -0.6 and 0.6. Hyper—hypermethylated CpGs; Hypo—hypomethylated CpGs. B Heatmap of the CDX2 DNA methylation pattern in the IM organoids vs. normal gastric organoids. The arrow indicates the transcriptional direction. CGI—CpG island, TSS—transcription start site, 5′UTR—5′ untranslated region, IGR—intergenic region. C ExE-hyper-CGI methylation of in healthy and precancerous samples. Shown are the mean ExE-hyper-CpG island methylation values per sample ranked by their means. Normal samples include all the samples from our mucosoid cultures (antrum, corpus and fundus) as well as all the healthy samples from the organoid and biopsy IM data sets [13] and the Barrett’s esophagus (BE) biopsy data sets [56]. The dashed red line indicates the upper 95% confidence interval limit of all normal samples. Diseased samples include the respective in vivo mild IM and IM (biopsies), IM (organoids) and BE (biopsies). D Venn diagram of genes with hypermethylated or hypomethylated promoter regions in diseased samples as compared to healthy samples. Diseased samples: IM (organoids), microsatellite instable (MSI), genomically stable (GS) and chromosomal instable (CIN) molecular subtypes of gastric cancer [14]. Tables indicate the number of differentially expressed genes among those shared by all three cancer subtypes and IM

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